Mlxipl, also known as carbohydrate-responsive element-binding protein, is an important regulator of glucolipid metabolism [2,4]. It is involved in the transcriptional regulation of lipogenic genes, which is crucial for fatty acid and fat synthesis in the liver, a process related to very low-density lipoprotein (VLDL) production and energy distribution [3]. Mlxipl has a wide-ranging impact on human health and disease, being associated with multiple physiological and pathological processes [5].

In prostate cancer, MLXIPL expressed in response to CD8+ T cell infiltration is associated with a poor prognosis, suggesting its role in tumor-related immune-microenvironment [1]. In hepatocellular carcinoma, MLXIPL levels are elevated. Knockdown of MLXIPL impedes HCC cell growth, invasion, migration, and glycolysis. It promotes the malignant progression of HCC by activating phosphorylation of mTOR [2]. Carriers of a common missense variant in MLXIPL, Gln241His, show significant associations with various lipid-related serum levels and a higher risk of steatotic liver disease (SLD), indicating its potential as a pharmacological target for SLD and hyperlipidemia [4]. In the spinal dorsal horn, after peripheral nerve injury, cJun-induced upregulation of Mlxipl inhibits microglial-derived neuroinflammation, counteracting mechanical allodynia [5].

In conclusion, Mlxipl plays essential roles in glucolipid metabolism, tumor progression, and neuropathic pain regulation. Studies on Mlxipl, especially through gene-based research models, have provided insights into its functions in various disease conditions, such as prostate cancer, hepatocellular carcinoma, steatotic liver disease, and neuropathic pain. These findings may contribute to the development of new therapeutic strategies for these diseases.